Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas
Brunton, C. (2016). Social interaction affects acquisition of lithium chloride-induced conditioned taste aversion: identification of underlying changes in neuronal activation in key forebrain areas (Thesis, Master of Science (Research) (MSc(Research))). University of Waikato, Hamilton, New Zealand. Retrieved from https://hdl.handle.net/10289/10641
Permanent Research Commons link: https://hdl.handle.net/10289/10641
A conditioned taste aversion (CTA) develops when exposure to a novel tastant is followed by sickness/malaise. Recently, it has been shown that a CTA can be reduced if the animal is placed in a social environment, i.e., in the presence of a conspecific, during the CTA acquisition phase. The current project was aimed to expand on our understanding of this phenomenon by (a) identifying the magnitude of an aversive response to a saccharin solution induced by lithium chloride (LiCl), a known emetic agent, in mice maintained in the social versus non-social setting; and (b) defining differences in LiCl-induced neuronal activation in the key CTA-related forebrain areas of animals in the social and non-social scenario. In mice lacking social stimulation, LiCl at a dose of 1 mEq induced a mild CTA to saccharin and the 6-mEq dose produced a profound aversive response. On the other hand, 6 mEq was the lowest effective dose in mice kept in the social setting. Immunohistochemical analysis of a neuronal activity marker, c-Fos, showed that alteration of activity in the paraventricular nucleus of the hypothalamus (PVN) and central nucleus of the amygdala (CEA) is associated with the observed changes. In LiCl-injected mice subjected to social stimulation, also the percentage of Fos-positive oxytocin (OT), but not vasopressin neurons in the PVN was higher than in LiCl-treated single-housed mice. These results are discussed in context of the effects that sociality has on the magnitude of responses to adverse associative stimuli and an involvement of specific elements of brain circuitry in mediating these effects.
University of Waikato
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